Researchers with the Western College of Veterinary Medicine have identified genetic markers that might help identify genetic lines that are more resistant to Porcine Reproductive and Respiratory Syndrome (PRRS). 
PRRS can result in early farrowing, the birth of weak infected pigs or death of the fetus but some fetuses within a litter or entire litters will escape infection. 
To identify strategies to keep sows from infecting their offspring, researchers are examining the mechanisms of fetal compromise. 
A Western College of Veterinary Medicine professor, Dr. John Harding said some fetuses resist infection better than others. However, the infection tends to be heterogeneous or uneven in the endometrium and clusters spatially within a litter so resilience might be a chance event. 
If the level of virus is low in the endometrium adjacent to a given fetus, it may simply delay the virus transmission.  
“We understand fetuses with intrauterine growth restrictions are resistant and have lower viral load than normal growth littermates.” 
Maybe because of a smaller placenta, perhaps less efficient nutrient exchange or lower rates of cell division affect the likelihood of infection. Or the amount of virus crossing the placenta or lower metabolic demands resulting in a more remarkable ability to withstand the adverse metabolic consequences of infection. 
There might also be a genotypic effect. 
“So, using a genomic approach, we have identified several genetic markers related to fetal resilience. We are exploring these in terms of specific genes involved and how any specific mutation or variant might change fetal metabolism to result in greater resilience.” 
Dr. Harding said the ultimate goal is to identify genetic factors considered in breeding programs or develop therapeutic interventions. 
While considering various mechanisms, they don’t fully understand how the virus crosses the placenta. However, their research shows the virus crosses the placenta very quickly and suggests using an easily accessible route to cross the placenta into the fetus. 
This might be hijacking an existing pathway supplying nutrients to the fetus or related to the regular movements of immune cells in and around the maternal and fetal sides of the placenta. The virus replicates in maternal immune cells and exists in the uterine endometrium or lining. 
We found lots of evidence of infected macrophages replicating virus adjacent to the maternal-fetal border, as well as what looked to be ‘free virus’ probably released from these macrophages upon their destruction. 
These macrophages are the virus factories that the virus uses to propagate while these immune cells conduct their normal surveillance activities in the maternal-fetal interface. 
Dr. Harding said the long-term goal of this work is to identify genetic factors to consider when developing breeding programs or therapeutic interventions. •
— By Harry Siemens